NBME 17 Block 3

Ans: E

Explanation
Ibutilide is a Class III antiarrhythmic drug. Most Class III antiarrhythmics are associated with Torsdaes de Pointes as a complication [FA2020 323]

Other drugs associated with Torsades de Pointes are drugs that induce prolonged QT including: Class IA antiarrhythmics, some antibiotics like macrolides, antipsychotics like haloperidol, TCAs, and some antiemetics like ondansetron [FA2020 p294].

Ans: E

Explanation
Answer from cassdawg:

Omeprazole is a proton pump inhibitor which affects the bioavailability of itraconazole presumably by interfering with absorption as it decreases gastric pH.
https://www.ncbi.nlm.nih.gov/pubmed/9626921
https://www.ebmconsult.com/articles/ppi-proton-pump-inhibitors-decrease-absorption-itraconazole

Answer from cheesetouch:

Azoles (including itraconazole) and omeprazole are both P450 inhibitors. (p450 interactions FA2018 P247, azoles FA2018 p199.

Ans: D

Explanation
TL;DR: The proper formation of granulomas to wall off TB requires CD4 Th1 cells and marcophages

TB (mycobacterium tuberculosis) begins its life cycle inside of the lungs by being phagocytized by alveolar macrophages abd undergoing intracellular growth and replication within the macrophages. NONactivated macrophages lack the ability to kill TB. In a normal person, some of the macrophages will present TB antigens to CD4 cells and secrete IL12, inducing differentiation to Th1 cells which will then begin the process of granuloma formation. No CD4 T-lymphocytes means no activation of macrophages for granuloma formation, so the macrophages will have deficient function.

FA2020 p217 has the steps of granuloma formation:

APCs present antigens to CD4 helper T-cells and secrete IL12 to cause differentiation into Th1 cells
Th1 cells secrete IFNgamma to activate macrophages and induce granuloma formation
Activated macrophages have better intracellular killing of pathogens such as TB and will increase cytokine secretion (e.g. TNFalpha) to cause formation of epitheliod macrophages and giant cells
TNFalpha is necessary for maintenance of granulomas

NOTE: Langhans giant cells are formed by activated macrophages after granuloma formation has been already been initiated

Ans: E

Explanation

Ans: C

Explanation
This individual has horizontal conjugate gaze palsy, likely intranuclear opthalmoplegia which is commonly a symptom of MS (hence her relapsing remitting history) [FA2020 p543]

Intranuclear opthalmoplegia can be caused by a lesion in the medial longitudinal fasciculus, which is located at "C" on the diagram. Here is a picture pointing out the MLF, which cooresponds to C on the diagram.

The Medial Longitudinal Fasciculus is what allows for cross-talk between CNVI and CNIII for conjugate gaze.

Ans: E

Explanation
FA2020 p116

Leukocyte adhesion deficiency presents with late separation of the umbilical cord, absence of pus (since pus is made of neutrophils), and dysfunctional neutrophils leading to recurrent skin and mucosal infection

LAD is due to a defect in LFA-1 integrin on phagocytes causing deficiency in adhesion and transmigration.

Ans: C

Explanation
Lichen sclerosus is a vulvular pathology involving thinning of the epidermis with fibrosis/sclerosing dermis, most commonly presenting with skin fragility (paper-thin) in post-menopausal women (FA2020 p644)

The other answers do not fit:

Candidal infection = itchyness and cottage cheese discharge; the excessive itching can lead to lichen sclerosus but would also be treated by the miconazole
HPV = genital warts or cervical cancer
Trichomoniasis = itchy with green smelly discharge, see organisms on microscopy
Urethral prolapse = rare, painful, would not cause these symptoms and would cause swelling in urethral area

Ans: D

Explanation
Aminoglycosides (like gentamycin) are bactericidal via irreversible inhibition of the initiation comblex by binding the 30S subunit [FA2020 p191]

Amoxicillin is a beta-lactam antibiotic which works by binding and inhibiting penicillin-binding proteins (transpeptidases) and block cross-linking in the cell wall [p187]
Ciprofloxacin is a bactericidal fluoroquinolone which acts by inhibiting DNA gyrase (topoisomerase II) and topoisomerase IV [p195]
Erythromycin is a macrolide (the macrolides are ACE - azithromycin, clarithromycin, and erythromycin) which acts by inhibiting protein synthesis via bindind to the 50S subunit and preventing translocation (macroslides) [p193]
Sulfamethoxazole is a sulfonamide which acts by inhibiting dihydropteroate synthase therfore inhibiting folate synthesis [p194]

Ans: B

Explanation

Visit the website link given below for futher explanation:-
https://freenbme.com/exam/nbme22/1316.html

Ans: B

Explanation
The question stem is referring to a conjugate vaccine. This is because conjugate vaccines convert T-independent antigens (polysaccharides) into T-dependent antigens by conjugating them with a protein.[FA2020 p127]

Remember that in order for a T-cell to be able to respond to an antigen via MHC, it MUST be a protein. Thus, T-dependent (dependent on T-cells) responses are to proteins. T-dependent responses are overall better because then B-cells can then undergo affinity maturation and class switching through interaction with T-cells. So, by conjugating bacterial polysaccharides to proteins, the immune response will be a more robust T-dependent reaction and will yield better protection. [FA2020 p103]

Conjugate vaccines exist for encapsulated bacteria (as the capsules are polysaccharide and would need to be conjugated to protein to improve response). These are Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae

You can remember these encapsulated organisms and their conjugate vaccine because they are THE SAME organisms that you become susceptible to when you have a splenectomy and which necessitate vaccination.

Ans: C

Explanation
Splenectomy is indicated for hereditary spherocytosis because it is an intrinsic hemolytic anemia where the spleen is destroying the red cells even though they could technically function fine. Thus splenectomy will prevent premature removal by the spleen (FA2020 p422).

Sickle cell disease causes autosplenectomy/splenic infarct/sequestration but splenectomy is not indicated because the spleen is not contributing to the symptoms of sickle cell, the symptoms are caused by the vasoocclusive disease.

Ans: B

Explanation

Answer to be searched by Sparsha Mehta

Ans: C

Explanation
The pt has sarcoidosis via the classic demographic association and the b/l hilar adenopathy

in sarcoid you get increased ACE and you also get hypercalcemia due to increased 1-alpha-hydroxylase (via acitvated macrophages) which leads to increased vitamin D

FA2020 pg 676

Ans: A

Explanation
6-month history of exertional chest pain that is relieved by rest = stable angina. Per FA2019, pg. 301--stable angina is usually secondary to atherosclerosis with more than 70% occlusion.

Contrary to what you might think (or at least this is doublethink for me!), plaques that occlude a larger percentage of the lumen are usually older and more stable (i.e. calcified) and this makes them less dangerous. These larger, older occlusions usually have a well-developed fibrous cap that makes them less likely to rupture and cause unstable angina/NSTEMI or STEMI.

B/c this guy has had symptoms that are not increasing in intensity over the past 6 months, he likely has a calcified, lg. plaque.

Ans: D

Explanation
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This has to do with the algorithm of treating shock. Septic (a type of distributive) shock as well as hypovolemic shock are treated with IV fluid resuscitation (FA2020 p310). Crystalloid fluids are first-line choice, and normal saline (0.9%, isotonic) is first-line specifically in cases of shock.

5% dextrose in water and 0.45% saline is hypertonic and not useful here.

5% dextrose alone is isotonic in the bag but physiologically hypotonic. It is more often given for fluid replacement after severe dehydration.

0.45% saline only is hypotonic and not useful here.

3% saline is hypertonic and not useful here.

Ans: D

Explanation
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FA 2018 p 290 - treat 3rd degr heart block with pacemaker

Ans: D

Explanation
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The most commonly used medications for erectile dysfunction are the phosphodiesterase inhibitors (specifically PDE5 inhibitors which include Sildenafil/Viagra). (FA2020p246)

PDE5 inhibitors (-afils) work by inhibiting the hydrolysis of cGMP by phosphidiesterase, increasing cGMP levels in smooth muscle cells causing relaxation/dilation and allowing the corpora cavernosa to fill with blood (viola, erection).

Ans: E

Explanation
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Thymoma is most commonly associated with myasthenia gravis as a paraneoplastic syndrome (FA2020 p228)

Myasthenia gravis is characterized by antibodies to the acetylcholine receptor and commonly presents with ptosis, diplopia, and ophtalmoplegia [p472]

Ans: E

Explanation
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1st Answer
This answer is honestly a joke. They want you to protect the pt's "fee fees" by allowing him to blame his weight on his genetics while also bringing in environmental factors so you can possibly segway into changing living habits.

2nd Answer
Most everything is a combination of genetics and environment. This is the only answer that acknowledges that even if the role is minor.

Ans: D

Explanation
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This is one of the main consequences of liver failure. [FA2020 p389]

The proposed mechanism is an imbalance in free testosterone and estrogen caused by defect in sex hormone binding globulin (more free estrogen = gynecomastia).

Ans: B

Explanation
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There are two types of infarcts : Pale infarcts - occurs in organs with a single end arterial blood supply
Red infarct ( also known as hemorrhagic ) - occurs in venous occlusion and tissues with multiple blood supplies ( eg liver , lung , intestine , testes )

Our patient clearly has a red infarct of the small intestine due to " mesenteric venous occlusion " .

The cause may very well be thrombosis secondary to a Polycthemia caused by his hepatocellular carcinoma( which secrete Erythropoietin) . Regardless of the cause however , we just had to recognise that this is a red infarct , and these are due to venous occlusion

Ans: A

Explanation
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Hormone sensitive lipase (HSL) is the enzyme which degrades triglycerides stored within adipocytes (FA2020 p93). Thus, it makes sense that it is activated in times of fasting and suppressed in the fed state.

Insulin would inhibit HSL, as insulin is a fed state enzyme secreted by the pancreas and would want to trigger storage of triglycerides.

In contrast glucagon is secreted in response to hypoglycemia by the pancreas and will trigger fasted state activation. In terms of the fed/fast state I always think of glucagon and epinephrine kind of like a superhero and their side kick, because they usually work together in the fasting state on similar targets to ensure the body has enough energy (this helps me remember that epinephrine and glucagon are fasting state hormones). Here though is epinephrine's big action away from glucagon, where glucagon has minimal effect and epinephrine has the big action of activating HSL! Glucagon has a minor role and other catecholamines and ACTH can also serve to activate HSL as well.

Another example of the synergistic work of glucagon and epinephrine is in glycogen breakdown (FA2020 p85). Both will trigger cAMP increase and protein kinase A activation which will phosphorylate glycogen phosphporylase and activate it (FAST PHOSPHORYLATE! Hormone sensitive lipase is actually phsophorylated to activate it as well).

FUN FACT: Hormone sensitive lipase actually got its name because it was sensitive to epinephrine!

Ans: E

Explanation
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The Congo Red staining showing characteristic birefringence (usually described as apple green) is indicative of amyloid (FA2020 p212). Her findings are characteristic of secondary amyloidosis with serum amyloid A which can cause restrictive cardiomyopathy and nephrotic syndrome and is associated with rheumatoid arthritis.

Amyloid protein composition is misfolded aggregates of beta-pleated sheets.

Ans: C

Explanation
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FA 2020 pg 425

Porphyria cutanea tarda-- defect in UROD in the heme synthesis pathway that causes photosensitivity and blistering

Ans: B

Explanation
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FA2020 p256

This would be a prospective cohort as they are looking at two groups with and without risk factors and assessing disease incidence.

UWorld has a super pretty picture which helps visually explain the differences (Copyright UWolrd, blah blah buy UWorld)

Ans: E

Explanation
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Tolterodine
Oxybutinin Muscarinic antagonists used for urinary urgency

Ans: D

Explanation
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The big hint here is EXTREME respiratory depression which is characteristic of opioid overdose, so he should be given naloxone. [FA2020 p570 has drug intoxication and withdrawal syndromes]

Ans: F

Explanation
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1st Answer
FA2020 p258

Odds ratio = (250/250) / (50/150) = 3

2nd Answer
odds ratio for the exposure variable (aniline dye) = (yes cancer and yes dye / yes dye) / (no cancer and yes dye / yes dye) = (250/250) / (50/150) = 3

Ans: A

Explanation
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1st Answer
I was thrown off because Pathoma/Dr. Sattar and pixorize say it is critical to start steroids ASAP to avoid permanent damage to the ophthalmic artery and blindness in patients suspected of having Giant Cell (Temporal) Arteritis.

This means not waiting for diagnostic confirmation.

However a 99% sensitivity does not equate to a 99% certainty of GCA/TA. So additional testing is the best answer choice even though her elevated ESR gives us strong suspicion of GCA/TA.

2nd Answer
Sensitivity of 99% means that almost all TA will have high ESR. (Sn = tp/(tp+fn) -> low False negative). HOWEVER, a specificity of just 60% means high ESR can indicate MANY OTHER disease processes. In a test with low specificity, more tests should be done to confirm diagnosis.

Ans: C

Explanation
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He has Huntington's disease (hence the irritability, depression, and chorea - sudden, jerky, purposeless movements) (FA2020 p520)

Huntington's is autosomal dominant so family history would be apparent.

Ans: B

Explanation
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This question is essentially asking what happens to sympathetic and parasympathetic efferents in the setting of hypovolemia/dehydration. In this setting, there would be lower blood pressure and thus this would cause reduced firing of the carotid baroreceptors, ultimately leading to feedback which stimulates the sympathetic nervous system (to increase heart rate and cause peripheral vasoconstriction in order to compensate for hypovolemia) while also inhibiting the parasympathetics.

Ans: B

Explanation
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I think that this is osteogenesis imperfecta based on the hx of several fractures that occurred during birth.

From FA2019, pg. 51: Manifestations can include--multiple fractures with bone deformities and minimal trauma; may occur during the birth process

OI is caused by gene defects in COL1A1 and COL1A2; most common form is autosomal dominant with decreased production of normal type 1 collagen.

Ans: C

Explanation
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Question describes the genetic concept of uniparental disomy ( inheriting both genes/ alleles from one parent )

Most cases of uniparental disomy will give a normal phenotype but in cases when imprinting is involved ( natural silencing of genes ) , abnormalities may occur . * Take for example the two most commonly cited examples of this situation

Prader -Willi and Angelman syndrome
In Prader Willi - normally the gene derived from mother(at that specific locus ) is silenced and it is the paternal allele which is functional. If the paternal gene becomes deleted , all you end up with a is the mothers silenced/nonfunctional allele . Alternatively if both genes are maternally derived ( Uniparental Disomy ) , you end up with 2 nonfunctional/silenced genes
The same thing occurs for angelman just vice-versa

Ans: E

Explanation
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Cyclosporine is an immunosuppressant that blocks T-cell activation by preventing IL-2 transcription (FA2020 p120)

Even without remembering the mechanism of cyclosporine, the answer could be inferred as most medications used after kidney transplant (cyclosporine, tacrolimus, sirolimus, basiliximab) block T-cell activation. This mechanism MAKES LOGICAL SENSE because T-cells are the primary mediators of acute rejection, which is what we are trying to prevent directly after a kidney transplant.

Ans: G

Explanation
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https://imgur.com/RQGrWLw

G represents the primary somatosensory area of the parietal lobe. The stem describes a 69 (nice) year old woman with sensory issues on the left side. She presents w/ a Babinski sign on the left, decreased somatic sensation in the left foot, agraphesthesia (when you "draw" a number on someone's skin and they can't interpret it) on the plantar surfaces of the toes, decreased position sense in the toes. The question says there is an edematous area in the cerebral cortex of the right hemisphere.

I had trouble with this, but I think it's describing somatosensory because of the sensory problems. Don't understand the UMN lesion (Babinski). Here's what Wikipedia says: "Lesions affecting the primary somatosensory cortex produce characteristic symptoms including: agraphesthesia, astereognosia, hemihypesthesia, and loss of vibration, proprioception and fine touch (because the third-order neuron of the medial-lemniscal pathway cannot synapse in the cortex). It can also produce hemineglect, if it affects the non-dominant hemisphere. Destruction of brodmann area 3, 1, and 2 results in contralateral hemihypesthesia and astereognosis."

Ans: D

Explanation
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From FA2019, pg. 553:

Schizoid personality = voluntary social withdrawal, limited emotional expression, content with social isolation. Hence, our patient who has never been sexually active and keeps in minimal contact with his family, but seems not to be depressed about lack of connection. He also shows minimal emotion when congratulated on his new job.

Other answers:

Antisocial = disregard for the rights of others with lack of remorse. Involves criminality, impulsivity, hostility, and manipulation. History of conduct disorder as a child.

Avoidant = hypersensitive to rejection and criticism, socially inhibited, timid, feelings of inadequacy. In contrast to schizoid personality, avoidant personality desires relationships with other people, but is so afraid that people won't like them that they have trouble forming relationships.

Borderline = unstable mood and interpersonal relationships, fear of abandonment, impulsivity, self-mutilation, suicidality.

Schizotypal = eccentric appearance, odd beliefs or magical thinking, interpersonal awkwardness; included on the schizophrenia spectrum.

Ans: B

Explanation
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This individual is suffering from hypocalcemia, which explains the seizures, twitching (reason for Chvostek sign - tapping of the facial nerve causing contraction of the muscles), and spasms (similar to Trousseau sign - inflation of the blood pressure cuff causing carpal spasm). It also may present with QT prolongation and numbness and tingling (as described). It is also important to note that though mild hypocalcemia causes hyporeflexia, extreme hypocalcemia can lead to hyperreflexia, tetany, parasthesias, and seizures (see here). Basically you cannot bank on the reflexes.

Hypercalcemia would present with stones (renal), bones(pain), groans(abdominal pain), thrones( urinary frequency), psychiatric overtones(anxiety, altered mental status).

The others answers are incorrect because:

Bicarbonate disturbances are related to acid/base imbalance and would not present with the symptoms described.
Chloride:
- Hypochloremia (associated with excessive vomiting) is typically accompanied by hyponatremia and typically presents with weakness/fatigue and dehydration.
- Hyperchloremia disturbances are generally related to kidney issues and when signs present they are dehydration, excessive thirst, fatigue, and dry mucus membranes
Potassium:
- Hypokalemia presents with muscle cramps, spasm, and weakness but also with cardiac anomalies (arrhythmias) and flattened T-waves on ECG.
- Hyperkalemia presents with wide QRS and peaked T waves on ECG, weakness, and arrhythmias.
Sodium:
- Hyponatremia can cause seizures and stupor, but it also typically presents with nausea and vomiting, weakness/fatigue, and confusion. Here is a good hyponatremia pneumonic (SALTLOSS - Stupor, Anorexia[nausea, vomiting], Lethargy, Tendon reflexes decreased, Limp muscles/weakness, Orthostatic hypotension, Seizures, Headache)
- Hypernatremia presents with irritability and stupor

Electrolyte Disturbances: FA2020 p591

Ans: D

Explanation
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Loratadine is a second generation antihistamine and thus would be preferred in this patient as it does not cause sedation. [FA2020 p686]

Since he works operating heavy machinery, it would be preferred to put him on a second generation antihistamine. Bropheniramine, hydroxyzine, and diphenhydramine are first generation antihistamines which cause sedation.

Ranitidine is a histamine H2 blocker used to decrease secretion by parietal cells in peptic ulcer disease, gastritis, and gastric reflux [FA2020 p399]

Ans: C

Explanation
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Cold temperature: Causes peripheral vasoconstriction and central vasodilation

Increased central blood volume --> Lower ADH due to increased blood volume through kidneys
Increased central blood volme --> leads to atrial stretching, increased preload --> Increased ANP release

Ans: B

Explanation
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This is Dissiminated Intravascular Coagulation (FA2020 p428)

DIC is a consumption coagulopathy (clotting factors are activated EVERYWHERE so they quickly produce microthombi and are consumed, allowing for bleeding). Thus, the individuals present with a consumption of coagulation factors leading to increased bleeding time, increased PT/INR, increased PTT, low fibrinogen and other clotting factors as well as a consumption of platelets leading to thrombocytopenia. Because there is widespread clotting factor activation, they also have signs of widespread microthombi sich as schistocytes and increased fibrin degradation products.

Ans: A

Explanation
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Figure from this paper shows the course of the inferior alveolar n.

https://www.ncbi.nlm.nih.gov/books/NBK546712/

Inferior alveolar n. is also sometimes called the inferior dental n. b/c it supplies sensation to the lower teeth.

Ans: A

Explanation
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I'm guessing the idea here is to not leave the patient hanging on what his diagnosis is and to answer his question directly.

Ans: B

Explanation
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The two most common defects in fatty acid metabolism are systemic primary carnitine deficiency and medium-chain acyl-CoA dehydrogenase deficiency or MCAD [FA2020 p89]. Both can present with physically normally appearing babies as the primary issues occur later (MCAD between 3 and 24 months and some variations of carnitine deficiency don't present until adolescence). Often the main danger is "hidden" in neonates unless prolonged fasting occurs because the individuals will go into hypoketotic hypoglycemic and can die. Thus, they are put on the newborn screens along with other disorders of fatty acid metabolism.

Thus, this neonate would have likely normal appearing physical exam and general labs. The best test of the list would be to look at acylcarnitine concentrations, which can be used to detect many disorders of fatty acid metabolism and some organic acidemias (https://neurology.testcatalog.org/show/ACRN)

Amino acids are not associated with fatty acid metabolism. ABG and electrolytes would likely be normal and would not be helpful in diagnosis. Lactic acid levels would be useful in neonates to give an idea of oxygen delivery to tissues, but is not useful here.

Ans: D

Explanation
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I don't like how they are asking this, but I think what they are getting at is that after the stent placement ("subsequent to the stent placement") there will be reperfusion injury to the myocardial tissue which occurs through free radical injury and therefore membrane lipid peroxidation is the best answer (FA2020 p210 mentions membrane lipid peroxidation as a mechansism of free radical damage and lists reperfusion injury after thrombolytic therapy as a type). Elevations in the cardiac enzymes I assume are because of the injury to the cells.

Ans: A

Explanation
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This is Neurofibromatosis Type I, which is an autosomal dominant disease (FA2020 p60, 525)

Even if you did not know this fact, you could likely guess autosomal dominant based on the inheritance pattern and general disease described. It is VERY COMMON in the family on one side (the mothers) and it did not skip a generation. Autosomal recessive skips generations. Mitochondrial with variable penetrance could be possible, but the disease pattern for mitochondrial are myopathies, metabolic, or optic neuropathy. X-linked would have ALL of the sons of the mother affected (whether it was dominant or recessive).

Ans: E
Explanation
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This lady likely has pelvic inflammatory disease. PID occurs when sexually transmitted bacteria travel from the vagina to the uterus, fallopian tubes, or ovaries.

Symptoms of PID include--pain in the lower abdomen and pelvis, abnormal vaginal discharge, abnormal vaginal bleeding, pain during intercourse, fever and/or chills, and painful/frequent urination.

Causes of PID most commonly include gonorrhea and chlamydia. Risk factors include sexual activity, esp. with multiple partners or without a condom. Having a history of PID or STI is also a risk factor for PID.

Complications of PID include: ectopic pregnancy, infertility, tubo-ovarian abscess.

Our patient has abdominal pain + fever + vaginal discharge + high WBC count. She also has a hx of ectopic pregnancy 1 year ago, which could mean she had a bout of PID, putting her at risk for a second.

https://www.mayoclinic.org/diseases-conditions/pelvic-inflammatory-disease/symptoms-causes/syc-20352594

Ans: E
Explanation
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From FA2020, pg. 381:

Tubular adenoma--> neoplastic; tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential; usually asymptomatic, may present with rectal bleeding. Hence our patient who has been undergoing evaluation for fecal occult blood.